If the mouse is deprived of auditory input during a sensitive period of early life, it develops both a neural and behavioral hypersensitivity to acoustic stimuli in later life. Neural, behavioral, and anatomical parallels occur between this condition in the mouse and hyperrecruitment deafness in man, and we hypothesize that this human pathological condition is also produced by disuse supersensitivity, caused by damage to inner ear structures. We propose to deprive the mouse of acoustic stimuli by acoustic trauma or temporary conduction deafness and to examine the developmental histological, behavioral, electrophysiological trends. Various interrelationships of these measures (damage to organ of Corti; gross and single cell recordings at all levels of the auditory peripheral and central nervous system, from threshold intensity to 130 db; acoustic startle responses and convulsions) will be examined in an attempt to determine causal relationships. This phenomena will also be examined in the visual system. As findings are made, we will be in a position to look for similar effects in humans with recruitment deafness.